Yasuyo Ohta

A dynamic analysis of chest wall motions with MRI in healthy young subjects.

The objective of this study was to analyse respiratory‐related motion of the chest wall with non‐invasive method.

Expression of Intercellular Adhesion Molecule-1 and Lymphocyte Function-Associated Antigen-1 on Alveolar Macrophages in the Acute Stage of Radiation-Induced Lung Injury in Rats

We investigated the expression of intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) on alveolar macrophages and on lung tissue in the early stage of radiation-induced lung injury. Cells in the bronchoalveolar lavage and lung tissue were obtained from rats at various times between 1 and 8 weeks after 20 Gy of 60Co gamma irradiation of a hemithorax. These specimens were stained immunohistochemically with anti-ICAM-1 and anti-LFA-1alpha monoclonal antibodies. The expression of these factors was compared with that of a control group. The total number of alveolar macrophages in the bronchoalveolar lavage was significantly reduced from 1 to 3 weeks, and the number of neutrophils was significantly increased 2 and 3 weeks after irradiation. ICAM-1 and LFA-1 expression on alveolar macrophages was significantly increased starting 1 week after irradiation. The expression of ICAM-1 and LFA-1 on lung tissue was not elevated up to 8 weeks after irradiation. In conclusion, the increased expression of ICAM-1 and LFA-1 on alveolar macrophages as early as 1 week after irradiation suggests that adhesion molecules play a role in the development of radiation-induced lung injury.

Ventilatory responses to hypercapnia and hypoxia following chronic hypercapnia in the rat.

This study investigated the effects of an 18 week exposure to 10% CO(2) in air on minute ventilation (V(E)), breathing pattern and the chemoresponiveness of rats to hypoxic and hyperoxic stimuli. We found that V(E) remained elevated over the 18 weeks. Nonetheless, the breathing pattern changed significantly. Tidal volume increased and the durations of inspiration and the total cycle decreased. After the sustained hypercapnia the mean Pa(CO(2)) was 72.0+/-5.1 (S. D.) mmHg. Every 6 weeks the chemoresponiveness of the CO(2)-exposed rats was tested by an acute exposure sequentially to room air, then a 6% O(2), 10% CO(2) and 84% N(2) gas mixture, and finally a 90% O(2) in 10% CO(2) mixture. On either room air or the hyperoxic-hypercapnic mixture V(E) fell to its pre-hypercapnic level. On the hypoxic-hypercapnic mixture V(E) increased significantly. These results demonstrate that the initial stimulating effect of 10% CO(2) on V(E) persisted for the entire 18 weeks without altering hypoxic or hyperoxic ventilatory responses.

Early damage to lung tissue after irradiation detected by the magnetic resonance T2 relaxation time.

We sought to determine whether nuclear magnetic resonance relaxation times of water in tissue would be useful to detect molecular damage in lung tissue within 2 weeks after irradiation. Tissue samples were obtained from the lungs of rats at various times between 1 and 14 days after exposure of a hemithorax to 20 Gy 60Co gamma irradiation. The spin-lattice relaxation time, T1, was measured by the inversion recovery method, and the spin-spin relaxation time, T2, was measured by both the Hahn spin-echo (Hahn T2) and the Carr-Purcell-Meiboom-Gill (CPMG T2) methods. The T2 of lung tissue could be divided into two components, T2 fast (T2f) and T2 slow (T2s), which reflected changes in the intracellular and extracellular water, respectively. The CPMG T2f increased significantly 3 days after irradiation (66.3 +/- 2.3 ms compared to 60.8 +/- 2.6 ms), and the CPMG T2s increased significantly 1 day after irradiation (155 +/- 11 ms compared to 138 +/- 7 ms), prior to the observation of abnormalities upon examination of the lung by light microscopy. The CPMG T2 values increased further up to 14 days after irradiation when significant increases were observed in values for T1, Hahn T2 and water content. Our results indicate that the molecular derangement in irradiated lung tissue was detected by the CPMG T2 measurement in the very early stage, and that MRI may be superior to conventional radiographs for detecting the early damage to lung tissue after irradiation.

MR appearance of pulmonary metastatic calcification

We report a case of metastatic pulmonary calcification that showed hyperintense signal on T1-weighted MRI. This uncommon MR appearance of calcification is similar to the MR characteristics of calcification in the brain due to abnormal calcium metabolism.

Furosemide Given by Inhalation Ameliorates Acute Exacerbation of Asthma

Previous studies have suggested that inhaled furosemide may have a protective effect against a wide variety of bronchoconstrictor agents, but a therapeutic effect has not been established in acute exacerbation of asthma. The purpose of this study was to investigate whether inhaled furosemide would exhibit any therapeutic benefit in acute asthma. We conducted a double-blind, placebo-controlled, randomized study in 40 patients with acute mild or moderate exacerbation of asthma. All patients received intravenous (i.v.) aminophylline 250 mg for 90 min and i.v. hydrocortisone 100 mg at entry. After randomization, 3 patients were excluded from the final analysis. At 30 min after starting i.v. aminophylline, 20 patients were given inhaled furosemide 20 mg and 17 patients received normal saline as placebo-control. Both inhalations were given by a jet nebulizer. The baseline forced expiratory volume at 1 sec (FEV1), peak expiratory flow rate (PEFR), and serum concentration of theophylline did not differ between the two groups. An increase in FEV1 in the furosemide group by 28.2 +/- 5.9% (mean +/- SE) was noted at 60 min, and this was significantly higher than in the control group. PEFR at 60 min was also significantly higher in the furosemide group than in control group. We conclude that inhaled furosemide has a bronchodilator effect on mild to moderate exacerbation of asthma when it is used with i.v. theophylline. Inhaled furosemide may benefit certain acute asthma patients, especially those suffering complications from the adverse effects of beta 2-agonists.

Rapid Response to Inhaled Frusemide in Severe Acute Asthma with Hypercapnia

We report 7 patients with severe acute asthma unresponsive to standard medication, including sympathomimetic agents, aminophylline and corticosteroids, who responded to inhaled frusemide. All were hypercapneic with a mean PaCO2 of 7.7 kPa (57.7 mm Hg) [range 6.2-8.8 kPa (46.2-66.3 mm Hg)]. Following nebulization of 20 mg frusemide, clinical response was rapid, and the mean PaCO2 fell significantly to 5.4 kPa (40.6 mm Hg) [range 5.0-6.2 kPa (37.5-46.5 mm Hg)] within 20-60 min. No adverse effect was recognized. Inhaled frusemide should be considered for treatment of acute asthma refractory to conventional therapy.

Distribution of pulmonary blood flow in conscious resting rats

The pattern of pulmonary blood flow (PBF) distribution was determined in the rat, in which lung gravitational forces are minimal. Microspheres were infused into the inferior vena cava of 15 conscious, and 5 anesthetized rats. Relative scatter of specific PBF [(sample activity/sample weight)/(total activity/total weight)] in 28 lung samples was calculated. In 5 of the conscious rats, consecutive determinations were made 30 min apart. In 5 anesthetized rats, PBF was determined in prone and supine positions. Relative scatter of specific PBF varied from 0.84 to 1.12, with PBF being distributed preferentially to the hilar, central regions. There was a high correlation between consecutive measurements: y = 0.88 x +0.11 (n = 140, r = 0.92). By changing from prone to supine position, PBF to the topmost regions increased, and that to the lowermost regions decreased, by only 3 percent. The results indicate that in the conscious resting rat, PBF has a small but significant preferential distribution to the hilar, central regions, with lower blood flow to the peripheral regions of the lung.

Differences in motor control in the bronchus and extrathoracic trachea

The motor control of the bronchus and extrathoracic trachea was evaluated by continuously measuring bronchial diameter and tracheal muscle tension as well as phrenic nerve activity in decerebrated, paralyzed, artificially ventilated dogs. Spontaneous rhythmic changes in bronchial diameter and tracheal muscle tension occurred in phase with phrenic burst during mechanical ventilation and during apnea induced by disconnecting the ventilator. There was a small but consistent difference in the timing of their rhythmic activities; bronchial constriction started at mid-inspiration, whereas tracheal contraction began just prior to the end of inspiration. Both were active in the post-inspiratory phase. Both hypercapnia and apnea caused an enhanced rhythmic constriction of the bronchus, while evoking a tonic contraction of the trachea. Intermittent electric stimulation of the efferent vagus nerves revealed that repetitive stimulation with a short intermission was necessary to evoke a sustained constriction of the bronchus, and that the bronchus could maintain the sustained constriction only transiently. These results indicate that the motor control of the bronchus and extrathoracic trachea are distinct. The central nervous system may contribute to the difference in timing of the contraction between tracheal and bronchial smooth muscle. However, the difference in response to electric stimulation of the nervus vagus may be attributed to the peripheral neuromuscular system.

Magnetic resonance relaxation times in acute hydrostatic pulmonary edema induced by noradrenaline in rats.

Models of pulmonary edema have been used to study the nuclear magnetic resonance (NMR) characteristics of lung water. Several investigators have measured changes in the relaxation times in the permeability type of pulmonary edema, but relatively few have measured relaxation times in the hydrostatic type of pulmonary edema. In this study we determined the characteristics of NMR relaxation times T1, T2 (Hahn spin-echo decay) and water content in acute hydrostatic pulmonary edema induced by noradrenaline administration in rats. Changes in T1 and T2 showed a significant prolongation in hydrostatic pulmonary edema. T2 decay curves for peripheral lung tissues were muldexponential and fit two components [T2 fast (T2f) and T2 Slow (T2s) ]. With two-component T2 analysis, T2s showed greater prolongation than did T2f. The increase in T2s was significantly correlated with an increase in water content, but the increase in the T2f value was not correlated with water content or with a change in T2s. The T2s component, which likely reflected changes in interstitial water, was more closely related than the T2f component to an increase in water content in hydrostatic pulmonary edema. Results suggested that regional changes in hydrostatic pulmonary edema may be evaluated by multicomponent T2 analysis.